Exam 2 pt 2 Flashcards by Ryan Angeles

Deadliest of all head injuries

Epidural hematoma

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Epidural hematoma

Arterial bleeding that fills cranial cavity very quickly, compressing brain tissue (High pressure bleed)

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Epidural hematoma often results in

brain injury and may lead to death (medical emergency)

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Subdural hematoma occurs

following rupture of vessel–usually vein–between brain and dura (low pressure bleed)

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3 types of subdural hematoma

Acute, subacute, and chronic

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Most dangerous type of subdural hematoma

Acute

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Time it takes for S&S of acute subdural hematoma to occur

Usually immediately

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Time it takes for S&S of subacute subdural hematoma to occur

Days to weeks

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Time it takes for S&S of chronic subdural hematoma to occur

Can take weeks

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Subarachnoid/intraparenchymal hemorrhage is a result of

blood pooling inside brain

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If subarachnoid/intraparenchymal hemorrhage is caused by trauma, it is usually accompanied by

DAI

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Nontraumatic causes of subarachnoid/intraparenchymal hemorrhage

AVM
Chronic HTN
Brain tumors
Blood thinners

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Subfalcal herniation

Herniation of the cingulate gyrus under the falx cerebri toward the opposite hemisphere

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Uncal herniation

Herniation of part of the medial temporal lobe through the tentorial notch and is pressing the midbrain against the tentorium

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Herniation causing decorticate posturing

Uncal herniation

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Herniation causing decerebrate posturing

Tonsilar herniation

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Decorticate posturing is due to

a lesion at the level of the midbrain separating the forebrain from the brainstem

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Tonsilar herniation

One tonsil of the cerebellum herniates through the foramen magnum, compressing the medulla against the margin of the foramen

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Decerebrate posturing is due to

lesion at the level of the lower brain stem separating the brain from the spinal cord

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Normal ICP

5-10 mmHg

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Etiology of stroke

Ischemic 80%

Hemorrhage 20%

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Etiology of TBI

MVA

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Signs and symptoms of stroke

Hemiplegia, unilateral, focal, neurologic

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Signs and symptoms of TBI

Bilateral, focal, diffuse

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Age in those with stroke

Old

Age in those with TBI

Young

Cost of severe stroke

$250,000

Cost of severe TBI

$4 mil

Recovery period for stroke

3-6 months

Recovery period for TBI

Years

Recovery pattern for stroke

Hypo- to hypertonicity

Recovery pattern for TBI

Rancho LOCF

Risk factors for stroke

Medical

Risk factors for TBI

Personality/lifestyle

Long term impairments/disability for stroke

Sensorimotor, cognitive

Long term impairments/disability for TBI

Cognitive, behavioral

Functional limitations for stroke

B/I ADL

Functional limitations for TBI

IADL

Permanent disability for stroke

70%

Permanent disability for TBI

90%

Reoccurrence for stroke

Low/medium 10%

Reoccurrence for TBI

High

Ability to predict outcome for stroke

Fair/good

Ability to predict outcome for TBI

Poor

Cerebral perfusion pressure

MAP-ICP

Normal CPP

70-100 mmHg

Do not treat if ICP is

Greater than 20-25

Medications used for increased ICP

Edema control Anticonvulsants: seizure prophylaxis Neuromuscular blockade/sedation

Types of meds for edema control (Increased ICP)

Osmotic diuretics Steroids Barbiturates (CNS depressant)

Other meds used for BI

Meds for agitation, seizures, and spasticity

Early signs of increased ICP: Consciousness

Confusion Lethargy Weakness Restlessness

Early sign of increased ICP: Pupil

Sluggish

Early signs of increased ICP:Vision

Blurred/diplopia/decreased acuity, papilledema

Early signs of increased ICP: Motor

Contralateral paresis

Early signs of increased ICP: Vital signs

Stable

Early signs of increased ICP: Additional findings

Headache, nausea, seizures, CN palsy

Late signs of increased ICP: Consciousness

Coma

Late signs of increased ICP: Pupil

Fixed/dilated

Late signs of increased ICP: Motor

Abnormal posturing | Flaccid if herniation

Late signs of increased ICP: Vital signs

Acute increase in ICP causes compression of the cerebral blood vessels Leads to cerebral ischemia Leads to increase systemic blood pressure over the vasomotor center with simultaneous decrease in HR/RR (Cushing's response)

Late signs of increased ICP: Additional findings

Headache Vomiting Changes in brain stem reflexes

3 types of cerebral edema

Vasogenic cytotoxic interstitial

Clinically most important type of cerebral edema

Vasogenic

How does vasogenic edema happen

Damage to BBB Leads to inflammation Leads to increase in permeability

How does vasogenic edema spread

Starts in area of injury and spreads and damages ipsilateral white matter

Focal neurologic deficits of vasogenic edema

Decrease in consciousness

How does vasogenic edema resolve

By slow diffusion

How does cytotoxic edema happen

Disruption of cellular metabolism BBB is intact Leakage of proteins and fluid from damaged blood vessels (grey matter)

What is interstitial edema

Rare non-communicating hydrocephalus

Breathing types

Cheyne-Stokes Kussmal Apneustic

Cheyne-Stokes

Periods of apnea followed by periods of hyperpnea

Kussmaul

Rhythmic, gasping, deep respiration associated with severe acidosis or coma

Apneustic

Prolonged slow inspirations, short expiratory phase

Cause of respiratory changes

Damage to respiratory centers (pons or upper medulla) | Removal of input from vagus nerve and pneumotaxic center in pons

Ventilator modes from most severe to least severe

Assist control Synchronized intermittent mandatory ventilation Continuous positive airway pressure (CPAP)

Assist control mode

Breathes for patient (ventilator overrides pt effort)

Synchronized intermittent mandatory ventilation mode

Breathes with patient (patient overrides ventilator)

Continuous positive airway pressure (CPAP) mode

Maintains open airway (patient must breathe on own)

PT role in ICU

Perform PT initial eval Gain and maintain a clear chest Prevent skin breakdown Prevent loss of ROM Stimulate consciousness Sits at bedside/co-treat, even if patient is comatose or in persistent vegetative state Part of team involved in family education

Minimally conscious state characteristics

``` Following simple commands Gestural yes/no responses Intelligible verbalizations Purposeful, non reflexive behavior Imaging: activation of appropriate CNS centers ```

Brain dead characteristics

``` No brain stem reflexes No response to pain No spontaneous respiration Flat EEG (not required) Usually confirmed by 2 independent physicians Organ donation possible ```

Persistent vegetative state characteristics

``` "disorder of consciousness" After 4 weeks of vegetative stage Brain stem function relatively intact Usually no ventilation Some response to simulation ```

Exam 2 pt 2 Flashcards

(82 cards)